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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Under appropriate conditions, deficiencies of certain minerals and vitamins as well as high intakes of dietary fat increase the toxicity of a given dose of lead in experimental animals. The severity of lead poisoning can also be increased by the consumption of either deficient or excessive levels of protein. Mineral deficiencies appear to have some of the most profound effects on lead toxicity, since the consequences of plumbism can be exaggerated by feeding diets low in calcium, phosphorus, iron, zinc, and in some cases, copper. Evidence for an antagonism between lead and nutritional levels of selenium is inconclusive. Vitamin E deficiency and lead poisoning interact to produce an anemia in rats that is more severe than that caused by either treatment alone. Lead apparently exerts a pro-oxidant stress on the red cell, thereby causing its accelerated destruction. One of the biochemical mechanisms of lead poisoning may be the disruption of normal membrane architecture, thereby leading to peroxidative damage. Epidemiological surveys have suggested a negative correlation between the poor nutritional status of children with regard to calcium and the concentration of lead in blood. Other examples of potential interactions of mineral status and lead poisoning in humans include the hypothesized hazards of soft water to public health in areas with lead plumbing and the possible role of mineral deficiencies in the etiology of pica. Experimental studies have shown that in some situations combined nutritional deficiencies can have an additive effect in potentiating lead toxicity.
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PMID:Lead toxicity and nutritional deficiencies. 51 Feb 31

In seven adult patients receiving fat-free total parenteral nutrition (TPN) for 4 to 8 weeks, weekly determinations of plasma fatty acids and total plasma tocopherols were made. Four patients were deficient in essential fatty acids, as defined by triene: tetraene ratio greater than 0.4, at the end of the second week of TPN. Six patients were deficient by the end of the third week and all seven were deficient by the end of the fifth week of TPN treatment. One patient who was deficient in both essential fatty acids and zinc developed a scaling, eczemoid dermatitis that disappeared within 3 weeks after cessation of TPN and resumption of oral feedings containing both fat and zinc. After resumption of oral feedings by three patients, the triene: tetraene ratio returned to normal within 2 weeks. The mean of total plasma tocopherols fell over a period of 7 weeks and in three individuals, reached levels generally associated with deficiency. There were not any obvious clinical manifestations of vitamin E deficiency.
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PMID:Essential fatty acid deficiency in adults receiving total parenteral nutrition. 82 4

In adult rats, the influence of vitamin E deficiency on zinc metabolism in general and specifically in 15 tissues was studied. After 50 days, we found evidence of vitamin E deficiency and at this time point we injected a tracer amount of 65Zn. During the next 18 days the zinc status was unaffected. The zinc metabolism, however, was altered: the apparent retention increased and the biological half life was prolonged. On day 68, the changes in various tissues varied. Some tissues were affected in zinc concentration (higher in plasma and spleen; lower in cerebrum, fur and tail), others in specific activity (higher in pancreas; lower in cerebellum). The different effects may reflect differences in tissue response on impairement, caused by vitamin E deficiency.
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PMID:Dietary vitamin E deficiency and zinc metabolism. 180 32

Nutritional assessments were measured in the sixteen long-term survivors who had undergone a massive resection of more than two-thirds of the small intestine or less than 170 cm of the remaining small intestine. Prealbumin, retinol binding protein and zinc in serum and arm muscle circumference were significantly lower than the normal range. Serum albumin had a tendency to correlate to the length of the remaining small intestine. Nutritional risk index had a correlation with the length of the remaining small intestine. In this study, nutritional assessments in the patients with a massive resection of the small intestine indicated to be in preclinical malnutritional state. This may support that supplementary nutritional therapy is necessary for such patients. In addition, we reported a patient with sensory polyneuropathy caused by vitamin E deficiency due to short bowel syndrome. The level of vitamin E was low in his serum, 294 micrograms/dl (normal: 1004 +/- 65) and in his red blood cells, 136 micrograms/dl (normal: 176 +/- 9). His symptom was markedly decreased within two weeks after the administration of large doses of vitamin E.
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PMID:[Nutritional assessments in the long-term survivors following massive resection of the small intestine]. 322 94

The role of protein and calorie deficiency in sickle cell disease remains poorly defined. While such features as growth retardation, impaired immune function, and delayed menarche do suggest a relationship between sickle cell disease and undernutrition, measurement of more direct nutritional parameters in these patients have yielded mixed results. Anthropometric measurements such as skinfold thickness are subnormal in many but not all reports. Serum protein levels are normal, but low values for serum lipids have been reported. Finally, one small study shows an improvement in both growth parameters and clinical course following caloric supplementation. A variety of micronutrient deficiencies have been suggested in sickle cell disease. Numerous case reports describing an exacerbation of the chronic anemia that was reversed by folic acid therapy led to routine folate supplementation. More recent studies have shown, however, that clinically significant folic acid deficiency occurs only in a small minority of sickle cell patients. Clearly, more work is necessary to define the cost/benefit ratio of routine folic acid supplementation. Pharmacological amounts of vitamin B6 and certain of its derivatives possess in vitro antisickling activities. Nevertheless, a small clinical trial failed to demonstrate any consistent hematologic effects of B6 supplementation. Several reports indicate that vitamin E levels are low in sickle erythrocytes. Since these abnormal red cells both generate excessive oxidation products and are more sensitive to oxidant stress, and because oxidants appear to play a role in ISC formation, vitamin E deficiency could well be linked to ISC formation and hemolysis. Small clinical trials, however, have again failed to produce a clear hematological response in sickle cell anemia. The role of zinc in sickle cell disease has received considerable attention. Though studies are generally small, most do support a relationship between sickle cell disease and zinc deficiency. Etiologic associations between zinc deficiency and such complications of sickle cell disease as poor ulcer healing, growth retardation, delays in sexual development, immune deficiencies, and high ISC counts have all been suggested. Most of these studies need further corroboration. Iron deficiency is now known to be a relatively common occurrence in sickle cell anemia, especially in children and pregnant women. The theoretical benefits of concomitant iron deficiency and sickle cell anemia remain to be proven in a controlled clinical trial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and sickle cell disease. 355 92

Plasma concentrations of alpha-tocopherol (vitamin E) and other analytes in Asian elephants (Elephas maximus) in Nepal were determined during typical work camp management of the elephants. Elephants foraged for food for 4-6 hr each day under the control of mahouts and were also provided daily with cut forage and supplements of unhusked rice, cane molasses, and salt. Blood samples were taken monthly for 1 yr without chemical restraint from 26 female elephants in four camps. Elephants were 6-60+ yr of age. Mean (+/-SEM) alpha-tocopherol concentration was 0.77+/-0.047 microg/ml, with a range of 0.23-1.57 microg/ml. Subadults had lower concentrations than did older elephants, and there were significant differences in mean concentrations from different camps and in mean monthly concentrations. Plasma alpha-tocopherol concentration appears to vary widely between individuals, and a single value of <0.3 microg/ml is not sufficient to diagnose incipient vitamin E deficiency. Mean (+/-SEM) plasma retinol (vitamin A) concentration was 0.063+/-0.003 microg/ml with a range of 0.01-0.12 microg/ml. Subadults had higher concentrations than did older elephants, and mean retinal values differed significantly among camps. Beta-carotene was not found in plasma. Twenty-five other analytes determined or derived were generally similar to those reported in other Asian and African (Loxodonta africana) elephants. Estimates of nutrient intake, based upon diet composition, suggested that dietary concentrations of zinc and sodium may have been marginal, but the absence of signs of any nutrient deficiencies indicates that dietary husbandry in these elephant camps was generally satisfactory.
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PMID:Plasma vitamin E and other analyte levels in Nepalese camp elephants (Elephas maximus). 980 97

The eye lens is subjected to many risk factors over time, which contribute to changes in its transparency, finally leading in combination to cataract development. Ultra violet (UV) radiation is regarded as one of the widespread risk factors contributing to cataract formation, for example in combination with nutritional deficiencies. Both factors possibly contribute to the high number of cataracts in the sunbelt region of the world. In this study, two essential nutritional factors were investigated in Brown Norway rats, zinc and vitamin E deficiencies, alone and in combination with UV-A and UV-B irradiation. Young female Brown Norway rats were put on a special diet for 10 weeks, either highly deficient in Zinc or in vitamin E. The diet was otherwise identical to the control diet. Two weeks after putting the animals on the diet, UV irradiation was started in some of the groups with mydriatic pupils with 3 irradiation sessions per week (UV-A 1 J/cm2; UV-B 0.2 J/cm2). Irradiation was continued until the end of the diet treatment period. Body weight and food consumption were established at weekly intervals, as well as slitlamp microscopy to monitor changes in anterior eye segment morphology. In addition changes in transparency of the cornea and lens have been monitored and evaluated with a Scheimpflug camera (Topcon SL-45) at baseline, and after 4 and 8 weeks of irradiation. After sacrifice of the animals, the lens wet weight as well as the activity of superoxide dismutase (SOD) were determined. Zinc deficiency alone led to an almost complete arrest of body weight increase. In the cornea, UV-A in combination with zinc or vitamin E deficiency did not have any interactive effects. The combination of UV-B and zinc deficiency showed subtractive instead of additive effects on corneal transparency and neovascularization. In the lens both deficiencies positively interacted with UV-A and UV-B by increasing the density of the capsular and cortical layers. The lens fresh weight was significantly lower in zinc-deficient animals additionally irradiated with UV-A or UV-B. The activity of SOD was significantly lower in the lenses of zinc- or vitamin E-deficient animals additionally irradiated with UV-B. The experiments presented clearly demonstrate that dietary zinc and vitamin E deficiencies do interact with UV radiation damage in the cornea and lens of Brown Norway rats.
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PMID:Experimental evidence for interactive effects of chronic UV irradiation and nutritional deficiencies in the lens. 1206 Dec 68

Vitamin E and zinc have a number of functions in common, including membrane stabilisation, antioxidant function and modulation of prostaglandin metabolism. Previous studies have shown vitamin E malabsorption during zinc depletion and it appears that there is an interaction between the two nutrients. In this study we have investigated whether vitamin E deficiency affects zinc and copper concentrations in experimental animals. Male Wistar rats were maintained on a vitamin E deficient diet for either 6 or 10 months. At the end of the experimental period all animals had undetectable plasma vitamin E levels and increased red cell fragility. Plasma zinc concentrations were significantly reduced in all vitamin E deficient animals compared to control rats (p<0.002) and copper levels were reciprocally elevated (p<0.002). It appears likely that decreased zinc levels may represent redistribution of circulating zinc to tissues and cells as a secondary antioxidant, or for membrane stabilisation or prostaglandin synthesis.
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PMID:The effect of dietary vitamin E deficiency on plasma zinc and copper concentrations. 1683 24

Aging is associated with declined immune function, particularly T cell-mediated activity, which contributes to increased morbidity and mortality from infectious disease and cancer in the elderly. Studies have shown that nutritional intervention may be a promising approach to reversing impaired immune function and diminished resistance to infection with aging. However, controversy exists concerning every nutritional regimen tested to date. In this article, we will review the progress of research in this field with a focus on nutrition factor information that is relatively abundant in the literature. While vitamin E deficiency is rare, intake above recommended levels can enhance T cell function in aged animals and humans. This effect is believed to contribute toward increased resistance to influenza infection in animals and reduced incidence of upper respiratory infection in the elderly. Zinc deficiency, common in the elderly, is linked to impaired immune function and increased risk for acquiring infection, which can be rectified by zinc supplementation. However, higher than recommended upper limits of zinc may adversely affect immune function. Probiotics are increasingly being recognized as an effective, immune-modulating nutritional factor. However, to be effective, they require an adequate supplementation period; additionally, their effects are strain-specific and among certain strains, a synergistic effect is observed. Increased intake of fish or n-3 PUFA may be beneficial to inflammatory and autoimmune disorders as well as to several age-related diseases. Conversely, the immunosuppressive effect of fish oils on T cell-mediated function has raised concerns regarding their impact on resistance to infection. Caloric restriction (CR) is shown to delay immunosenescence in animals, but this effect needs to be verified in humans. Timing for CR initiation may be important to determine whether CR is effective or even beneficial at all. Recent studies have suggested that CR, which is effective at improving the immune response of unchallenged animals, might compromise the host's defense against pathogenic infection and result in higher morbidity and mortality. The studies published thus far describe a critical role for nutrition in maintaining the immune response of the aged, but they also indicate the need for a more in-depth, wholestic approach to determining the optimal nutritional strategies that would maintain a healthy immune system in the elderly and promote their resistance to infection and other immune-related diseases.
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PMID:The role of nutrition in enhancing immunity in aging. 2250 Feb 73

Cataract (opacity of the lens) and age-related degeneration of the macula of the retina are very common causes of disability in old age, and people are living longer. It seems likely that both of these conditions result from gradual photo-oxidative damage. The proteins in cataractous lenses are oxidized and 50 per cent of the fatty acids in membranes of retinal photo-receptors are highly polyunsaturated. The eye normally has unusually high concentrations of vitamin C and zinc which could have protective functions against free radical damage. For cataracts five reported case-control studies are reviewed and two prospective studies one of which included a very large number of subjects. Vitamin intakes were estimated from dietary histories or blood levels. In five of the six studies in which vitamin C was measured it appeared to be protective and vitamin E and carotenoids appeared protective in 5/7 studies. Other descriptive epidemiological studies are going on, including one in the Blue Mountains near Sydney. It is concluded that controlled trials of antioxidant nutrients for cataract prevention are now warranted. As to age-related muscular degeneration (ARMD), severe vitamin E deficiency is known to cause (a different type of) retinal degeneration spontaneously in humans (with cystic fibrosis or abetalipoproteinaemia) and experimentally in animals. Only three human case-control studies of ARMD and diet have been reported thus far and no clear relationship with any particular nutrient has emerged yet. Supplements containing antioxidant vitamins and zinc are being advertised and used in the USA and elsewhere but this is ahead of the evidence. More observational studies are needed and the US National Eye Institute is planning a 10 year intervention study, known as AREDS (Age-Related Eye Disease Study).
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PMID:Nutrients and degenerative eye diseases. 2439 83


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